Fluid state and blood pressure control in patients on maintenance hemodialysis

Abstract

Cardiovascular disease is the main cause of high mortality in dialysis patients. Hypertension is a risk factor for cardiovascular disease and despite the use of highly efficient antihypertensive drugs (AHD), blood pressure (BP) is poorly controlled in the vast majority of hemodialysis (HD) patients. The pathogenesis of dialysis-associated hypertension is multifactorial, but the fluid state is a dominant factor for control of BP. The assessment of an optimal fluid state, so-called dry weight (DW), is usually based on clinical observations and other methods for evaluation of fluid state such as ultrasound of the inferior vena cava diameter (IVCD) and plasma levels of atrial natriuretic peptide (ANP).

The aims of the present study were to:

1. evaluate the utility of IVCD measurements and ANP in assessing DW in maintenance HD (I, II).

2. determine whether endogenous plasma Asymmetrical Dimethyl Arginine (ADMA, an inhibitor of NO release) plays a role in the pathogenesis of dialysis-associated hypertension (III).

3. determine whether control of extracellular volume (ECV) is associated with normotension in HD patients (IV-V).

IVCD values and their changes during and 2 hours after HD were compared to those in BV, measured with radioisotopes and monitored continuously (I). Pre- and postdialysis ANP levels were compared to BV, IVCD and vasoactive hormones (II). ADMA was determined in HD and CAPD patients and related to BP (III). The fluid state was evaluated with bioimpedance, ultrasound of IVCD and continuous monitoring of BV and compared in normotensive HD patients treated with long and short HD and in hypertensive patients treated with short HD (IV). The effect of intensified fluid removal during 3 months on BP (48h BP monitoring) and AHD was assessed in 16 hypertensive HD patients (IV).

The main findings are:

1. IVCD measured at the end of or shortly after HD may be misleading in assessing DW due to fluid shift from the interstitial to the intravascular compartment which, in some cases, is not completed until 2 or more hours after HD. This time-lag limits the practical applicability of the method (I).

2. ANP release during HD is influenced by factors other than those related to changes in intravascular volume, such as age, presence of heart disease and possible interaction with other hormones, such as vasopressin and noradrenaline and its plasma levels are not useful for assessing the fluid state (II).

3. Plasma ADMA levels in dialysis patients are lower than those that might cause vasoconstriction due to inhibition of NO release. It is doubtful whether ADMA plays a significant role in the pathogenesis of dialysis-associated hypertension (III).

4. The normotensive patients treated with long and short HD had a similar fluid state and BP which were significantly lower than those in the hypertensive patients (IV).

5. We were able to reduce significantly ECV in 10 patients (group 1), but not in 6 patients (group 2). There was significant reduction in BP, especially during the night as well as in the dose of AHD in group 1. In group 2, BP and AHD dose remained unchanged (V).

We concluded that fluid overload plays a major role in the pathogenesis of dialysis-associated hypertension. Its removal leads to improve the control of BP and its diurnal rhythm with little, if any, AHD. Normotension in HD patients may be achieved independently of the duration and dose of HID, if the control of postdialysis ECV is adequate. However, this is more difficult to achieve with short than with long HD, during which the UF rate is slower, the BV change smaller and intradialytic symptoms less common. There is no "gold standard" for the assessment of DW in patients on maintenance HD. All methods proposed have limitations and careful and continued clinical evaluation of the patient remains the method of choice for assessing DW.